| First Author | Yoo SA | Year | 2019 |
| Journal | Nat Immunol | Volume | 20 |
| Issue | 10 | Pages | 1348-1359 |
| PubMed ID | 31406382 | Mgi Jnum | J:282374 |
| Mgi Id | MGI:6380735 | Doi | 10.1038/s41590-019-0456-4 |
| Citation | Yoo SA, et al. (2019) Placental growth factor regulates the generation of TH17 cells to link angiogenesis with autoimmunity. Nat Immunol 20(10):1348-1359 |
| abstractText | Helper T cells actively communicate with adjacent cells by secreting soluble mediators, yet crosstalk between helper T cells and endothelial cells remains poorly understood. Here we found that placental growth factor (PlGF), a homolog of the vascular endothelial growth factor that enhances an angiogenic switch in disease, was selectively secreted by the TH17 subset of helper T cells and promoted angiogenesis. Interestingly, the 'angio-lymphokine' PlGF, in turn, specifically induced the differentiation of pathogenic TH17 cells by activating the transcription factor STAT3 via binding to its receptors and replaced the activity of interleukin-6 in the production of interleukin-17, whereas it suppressed the generation of regulatory T cells. Moreover, T cell-derived PlGF was required for the progression of autoimmune diseases associated with TH17 differentiation, including experimental autoimmune encephalomyelitis and collagen-induced arthritis, in mice. Collectively, our findings provide insights into the PlGF-dictated links among angiogenesis, TH17 cell development and autoimmunity. |
